Exposure to Sodium Hypochlorite or Cigarette Smoke Induces Lung Injury and Mechanical Impairment in Wistar Rats.

Pulmonary irritants, such as cigarette smoke (CS) and sodium hypochlorite (NaClO), are associated to pulmonary diseases in cleaning workers. We examined whether their association affects lung mechanics and inflammation in Wistar rats. Exposure to these irritants alone induced alterations in the lung mechanics, inflammation, and remodeling. The CS increased airway cell infiltration, acid mucus production, MMP-12 expression, and alveolar enlargement. NaClO increased the number of eosinophils and macrophages in the bronchoalveolar lavage fluid, with cells expressing IL-13, MMP-12, MMP-9, TIMP-1, and iNOS in addition to increased IL-1ß and TNF-α levels. Co-exposure to both irritants increased epithelial and smooth muscle cell area, acid mucus production, and IL-13 expression in the airways, while it reduced the lung inflammation. In conclusion, the co-exposure of CS with NaClO reduced the pulmonary inflammation, but increased the acidity of mucus, which may protect lungs from more injury. A cross-resistance in people exposed to multiple lung irritants should also be considered.

Airway inflammatory profile among cleaning workers from different workplaces.

BACKGROUND: Cleaning workers represent a significant proportion of the active population worldwide, with poor remuneration, particularly in developing countries. Despite this, they remain a relatively poorly studied occupational group. They are constantly exposed to agents that can cause symptoms and respiratory problems. This study aimed to evaluate upper airway inflammation in professional cleaning workers in three different occupational settings by comparing nasal cytology inflammation and clinical profiles. METHODS: We performed a cross-sectional study on the prevalence of upper airway inflammation and symptoms of asthma/rhinitis related to cleaning work, according to workplace. A total of 167 participants were divided into four groups: hospital, university, housekeeper and control. A nasal swab was collected for upper airway inflammation evaluation. Clinical profiles and respiratory symptom employee evaluations were performed using specific questionnaires (European Community Respiratory Health Survey-ECRS and the International Study of Asthma and Allergies in Childhood-ISAAC). RESULTS: Cleaning workers showed increased neutrophils and lymphocytes; the hospital and university groups showed increased macrophages compared to the housekeeper and control groups. The hospital and housekeeper groups showed increased eosinophils when they performed cleaning services for up to one year and reported having more asthma symptoms than the control group. Cleaning workers showed increased rhinitis symptoms. The university group showed increased rhinitis symptoms aggravated by the workplace compared with the hospital and housekeeper groups. Cleaning workers showed an increased affirmative response when directly asked about rhinitis symptoms compared to the control group. CONCLUSIONS: Cleaning workers showed airway inflammation, asthma symptoms and rhinitis, regardless of the occupational environment to which they were exposed, as well as showed increased rhinitis and asthma symptoms. Hospital cleaning workers showed increased macrophages, lymphocytes and eosinophils compared to the others. The length of time spent performing cleaning work was not related to nasal inflammation or respiratory symptoms in this population. However, there were differences in workplaces. Registered on ClinicalTrials.gov. TRIAL REGISTRATION NUMBER: NCT03311048. Registration date: 10.16.2017. Retrospectively registered.

Clinical, functional and inflammatory evaluation in asthmatic patients after a simple short-term educational program: a randomized trial.

This study aimed to evaluate the clinical evolution, functional parameters and inflammatory activity of asthma in patients who submitted to an educational intervention. 58 adult patients over 18 years of age with partly controlled and uncontrolled asthma were randomized into an intervention group (IG) (N = 32) and a control group (CG) (N = 26) and evaluated for 12 weeks. The Asthma Control Test (ACT), Asthma Control Questionnaire (ACQ), Asthma Quality Life Questionnaire (AQLQ) and Beck Depression Inventory (BDI) questionnaires were applied. Spirometry, exhaled nitric oxide (NO), exhaled breath condensate (EBC) and induced sputum (IS), measurement of the peak flow and symptoms were performed. The IG patients received an educational activity for 30 min applied by a nurse. Statistical analysis: analysis of variance with repeated intragroup measures. IG presented a decreased number of eosinophils in IS and IL-17A in EBC, an increase in the percentage of FEV1 before and after bronchodilator and an improvement in quality of life compared to the CG. There was an improvement in depression levels and a decrease in IL-4 and IL-5 in the IS and in the EBC in both groups. Our results suggest that an educational intervention can bring benefits concerning the control of inflammation, lung function alterations, quality of life and levels of depression in asthmatic patients. Registration: ClinicalTrials.gov; NCT03655392.

Impairment on Cardiopulmonary Function after Marathon: Role of Exhaled Nitric Oxide.

BACKGROUND: The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morphofunctional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. PURPOSE: The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (eNO) and pulmonary inflammation. METHODS: 31 male marathoners, age 39 ± 9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; eNO analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. RESULTS: Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in eNO concentration (20 ± 11 to 35 ± 19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9 ± 12 e 12 ± 9 ppb, p < 0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p < 0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57 ± 6 to 55 ± 6 mL·min-1·Kg-1 and 134 ± 19 to 132 ± 18 Lpm, respectively, p < 0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in eNO 24 and 72 hours after marathon (r = -0.4, p = 0.05). CONCLUSION: Reduction in eNO bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon.

Impairment on cardiopulmonary function after marathon: role of exhaled nitric oxide

BACKGROUND: The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morpho functional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. PURPOSE: The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (Eno) and pulmonary inflammation. METHODS: 31 male marathoners, age 39 ± 9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; Eno analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. RESULTS: Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in Eno concentration (20 ± 11 to 35 ± 19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9 ± 12 e 12 ± 9 ppb, p < 0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p < 0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57 ± 6 to 55 ± 6 mL·min-1·Kg-1 and 134 ± 19 to 132 ± 18 Lpm, respectively, p < 0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in Eno 24 and 72 hours after marathon (r = -0.4, p = 0.05). CONCLUSION: Reduction in Eno bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon. (AU)